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Toxins
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Conotoxins: Novel Pharmacologies for Nervous System Disorders
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Conotoxins: Novel Pharmacologies for Nervous System Disorders

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Marine and Freshwater Toxins".

Deadline for manuscript submissions: closed (15 August 2015) | Viewed by 30772

Special Issue Editor

Prof. Dr. Macdonald Christie

E-Mail Website
Guest Editor
Discipline of Pharmacology, The University of Sydney, Sydney, NSW, Australia
Interests: Pain; Neuropathic pain; Conotoxins; Opioids; Neurotransmission

Special Issue Information

Dear Colleagues,

The more than 700 hundred species within the marine snail genus Conus, produce a vast array of peptide toxins, conotixns, both to immobilize prey and for defence. Only a small proportion of the conotoxins known to be expressed by Conus species have been fully characterized, but these have already produced a rich potential for therapeutic development and experimental tools. The conotoxins isolated, characterized and synthesized so far, exhibit highly specific interactions with a range of nervous system excitability molecules, particularly ion channels. A number of conotoxins that inhibit signalling proteins expressed selectively in pain pathways are under development as novel pain therapeutics. Ziconitide, an N-type voltage-gated calcium channel (Cav2.2) antagonist was approved by the FDA for management of severe chronic pain in 2004. Since then, conotxins interacting with a number of other novel pain targets have been developed, such as a group of α-conotoxins with novel mechanisms of action in addition to nicotinic acetylcholine receptor inhibition, noradrenaline transport inhibitors and specific sodium channel inhibitors. Considerable conotoxin research is also focussed on improving synthesis, stability, tissue distribution and bioavailability. Potential applications of contoxins are not limited to pain, with potential for treatment of Parkinson’s disease, Alzheimer’s disease, etc. Conotoxins are useful not only as therapeutics but, because of their remarkable selectivity for ion channel subtypes, they are useful research tools for identifying novel drug targets. This Special Issue will focus on original articles and reviews covering all aspects of conotoxin research with a particular focus on novel pharmacological properties and potential for application in treatment of pain and other nervous system disorders.

Prof. Dr. MacDonald Christie
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


Keywords

  • conotoxins
  • receptor and signalling mechanisms
  • structure and function
  • targeted therapeutics
  • pain
  • nervous system

Published Papers (4 papers)

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Research

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3925 KiB  
Article
Apoptosis Activation in Human Lung Cancer Cell Lines by a Novel Synthetic Peptide Derived from Conus californicus Venom
by Irasema Oroz-Parra, Mario Navarro, Karla E. Cervantes-Luevano, Carolina Álvarez-Delgado, Guy Salvesen, Liliana N. Sanchez-Campos and Alexei F. Licea-Navarro
Toxins 2016, 8(2), 38; https://doi.org/10.3390/toxins8020038 - 05 Feb 2016
Cited by 25 | Viewed by 7296
Abstract
Lung cancer is one of the most common types of cancer in men and women and a leading cause of death worldwide resulting in more than one million deaths per year. The venom of marine snails Conus contains up to 200 pharmacologically active [...] Read more.
Lung cancer is one of the most common types of cancer in men and women and a leading cause of death worldwide resulting in more than one million deaths per year. The venom of marine snails Conus contains up to 200 pharmacologically active compounds that target several receptors in the cell membrane. Due to their diversity and specific binding properties, Conus toxins hold great potential as source of new drugs against cancer. We analyzed the cytotoxic effect of a 17-amino acid synthetic peptide (s-cal14.1a) that is based on a native toxin (cal14.1a) isolated from the sea snail Conus californicus. Cytotoxicity studies in four lung cancer cell lines were complemented with measurement of gene expression of apoptosis-related proteins Bcl-2, BAX and the pro-survival proteins NFκB-1 and COX-2, as well as quantification of caspase activity. Our results showed that H1299 and H1437 cell lines treated with s-call4.1a had decreased cell viability, activated caspases, and reduced expression of the pro-survival protein NFκB-1. To our knowledge, this is the first report describing activation of apoptosis in human lung cancer cell lines by s-cal14.1a and we offer insight into the possible mechanism of action. Full article
(This article belongs to the Special Issue Conotoxins: Novel Pharmacologies for Nervous System Disorders)
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Review

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539 KiB  
Review
Conotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel Inhibition
by Nehan R. Munasinghe and MacDonald J. Christie
Toxins 2015, 7(12), 5386-5407; https://doi.org/10.3390/toxins7124890 - 10 Dec 2015
Cited by 15 | Viewed by 6245
Abstract
Chronic pain creates a large socio-economic burden around the world. It is physically and mentally debilitating, and many suffers are unresponsive to current therapeutics. Many drugs that provide pain relief have adverse side effects and addiction liabilities. Therefore, a great need has risen [...] Read more.
Chronic pain creates a large socio-economic burden around the world. It is physically and mentally debilitating, and many suffers are unresponsive to current therapeutics. Many drugs that provide pain relief have adverse side effects and addiction liabilities. Therefore, a great need has risen for alternative treatment strategies. One rich source of potential analgesic compounds that has immerged over the past few decades are conotoxins. These toxins are extremely diverse and display selective activity at ion channels. Voltage gated sodium (NaV) channels are one such group of ion channels that play a significant role in multiple pain pathways. This review will explore the literature around conotoxins that bind NaV channels and determine their analgesic potential. Full article
(This article belongs to the Special Issue Conotoxins: Novel Pharmacologies for Nervous System Disorders)
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1299 KiB  
Review
Bioactive Mimetics of Conotoxins and other Venom Peptides
by Peter J. Duggan and Kellie L. Tuck
Toxins 2015, 7(10), 4175-4198; https://doi.org/10.3390/toxins7104175 - 16 Oct 2015
Cited by 26 | Viewed by 7850
Abstract
Ziconotide (Prialt®), a synthetic version of the peptide ω-conotoxin MVIIA found in the venom of a fish-hunting marine cone snail Conus magnus, is one of very few drugs effective in the treatment of intractable chronic pain. However, its intrathecal mode of delivery and [...] Read more.
Ziconotide (Prialt®), a synthetic version of the peptide ω-conotoxin MVIIA found in the venom of a fish-hunting marine cone snail Conus magnus, is one of very few drugs effective in the treatment of intractable chronic pain. However, its intrathecal mode of delivery and narrow therapeutic window cause complications for patients. This review will summarize progress in the development of small molecule, non-peptidic mimics of Conotoxins and a small number of other venom peptides. This will include a description of how some of the initially designed mimics have been modified to improve their drug-like properties. Full article
(This article belongs to the Special Issue Conotoxins: Novel Pharmacologies for Nervous System Disorders)
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697 KiB  
Review
Conotoxin Interactions with α9α10-nAChRs: Is the α9α10-Nicotinic Acetylcholine Receptor an Important Therapeutic Target for Pain Management?
by Sarasa A. Mohammadi and MacDonald J. Christie
Toxins 2015, 7(10), 3916-3932; https://doi.org/10.3390/toxins7103916 - 28 Sep 2015
Cited by 39 | Viewed by 8474
Abstract
The α9α10-nicotinic acetylcholine receptor (nAChR) has been implicated in pain and has been proposed to be a novel target for analgesics. However, the evidence to support the involvement of the α9α10-nAChR in pain is conflicted. This receptor was first implicated in pain with [...] Read more.
The α9α10-nicotinic acetylcholine receptor (nAChR) has been implicated in pain and has been proposed to be a novel target for analgesics. However, the evidence to support the involvement of the α9α10-nAChR in pain is conflicted. This receptor was first implicated in pain with the characterisation of conotoxin Vc1.1, which is highly selective for α9α10-nAChRs and is an efficacious analgesic in chronic pain models with restorative capacities and no reported side effects. Numerous other analgesic conotoxin and non-conotoxin molecules have been subsequently characterised that also inhibit α9α10-nAChRs. However, there is evidence that α9α10-nAChR inhibition is neither necessary nor sufficient for analgesia. α9α10-nAChR-inhibiting analogues of Vc1.1 have no analgesic effects. Genetically-modified α9-nAChR knockout mice have a phenotype that is markedly different from the analgesic profile of Vc1.1 and similar conotoxins, suggesting that the conotoxin effects are largely independent of α9α10-nAChRs. Furthermore, an alternative mechanism of analgesia by Vc1.1 and other similar conotoxins involving non-canonical coupling of GABAB receptors to voltage-gated calcium channels is known. Additional incongruities regarding α9α10-nAChRs in analgesia are discussed. A more comprehensive characterisation of the role of α9α10-nAChRs in pain is crucial for understanding the analgesic action of conotoxins and for improved drug design. Full article
(This article belongs to the Special Issue Conotoxins: Novel Pharmacologies for Nervous System Disorders)
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